Pg. Rowland et al., COMPARATIVE-STUDY OF THE ADHESION OF SICKLE CELLS AND MALARIAL-PARASITIZED RED-CELLS TO CULTURED ENDOTHELIUM, The Journal of laboratory and clinical medicine, 121(5), 1993, pp. 706-713
Increased adhesion of red cells to vascular endothelium has been impli
cated in the pathogenesis of falciparum malaria and sickle cell diseas
e. We have carried out a comparative study of the adhesiveness of norm
al (AA), sickle trait (AS), and homozygous sickle (SS) red cells, with
and without parasitization by Plasmodium falciparum, with an in vitro
flow system. Adhesion of nonparasitized red cells to cultured human u
mbilical vein endothelial cells (either glutaraldehyde fixed or untrea
ted) was strongly dependent on the wall shear stress. Many AA and SS c
ells adhered at low stress (0.02 Pa), but far fewer did so when the st
ress was increased to a physiologic level (0.1 Pa). Compared with AA c
ells, SS cells adhered in greater number (about threefold) and require
d greater stress (about two-fold) for their subsequent removal. In con
trast, the efficiency of adhesion of AA cells parasitized by Plasmodiu
m falciparum was essentially constant up to 0.1 Pa, where it was about
1000 times greater than the efficiency for nonparasitized cells. The
stress required to remove parasitized cells was about 6 times that for
controls. When parasites were grown in SS cells, fewer cells adhered
than when parasites were grown in AA cells. However, the adhesion of m
alarial-parasitised AS cells was only slightly less than that of paras
itized AA cells, so that modulation of adhesion is unlikely to underli
e the protective effect of the sickle gene in malaria. Adhesion of red
cells to endothelium may promote blockage of microvessels, and the in
teraction of parasitized cells appears strong enough to directly cause
ischemic complications in falciparum malaria.